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NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS
Official Journal of the Bulgarian Society of Neurosonology and Cerebral Hemodynamics
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Search Results for “search_doc_txt.php” – NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS
Search in texts for 'circle of Willis' - Neurosonology.net'
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texts with exact phrase : '
circle of Willis
'.
1.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2006, No. 2
,
,
,
To compare cerebral autoregulation and collateral circulation in the different parts
of
the
circle
of
Willis
.
To compare cerebral autoregulation and collateral circulation in the different parts of the circle of Willis.
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2.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 3, 2007, No. 1
,
,
,
(2) Mechanism
of
equalizing the pressure
of
four channels by the
circle
of
Willis
.
The whole cerebral circulation system essential variable is again the blood flow. It is maintained by varying P and R, but here are valid some more principles and mechanisms: (1) Security on the basis of multiplicity (multiple line of performance e.g. multiple channels of supply), instead on the basis of perfect functioning of one line (there are four cerebral blood flow magistrals, two carotid and two vertebral).
(2) Mechanism of equalizing the pressure of four channels by the circle of Willis.
The anterior and the two posterior communicating arteries in which the flow is on 0-point in case of equal pressure in the four magistrals, automatically opened when the pressure differs. (3) Mechanism of compensation, through collateral systems (external carotid
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3.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 5, 2009, No. 1
,
,
,
To make good treatment decisions, early, reliable information about the condition
of
the arteries
of
the
Circle
of
Willis
is necessary [11].
The results obtained from a multicenter, openlabel, randomized cross-over study investigating the diagnostic potential of SonoVue using transcranial color-coded duplex sonography (TCCS) confirm this clinical observation [10]. In a group of forty patients, echo enhancement contributed to converting a non-diagnostic study into a diagnostic one in more than half of the indications (in 66%), and increased the confidence in diagnosis in 74 %. In a non-trial situation, this would have allowed the diagnosis to be reached more quickly.
To make good treatment decisions, early, reliable information about the condition of the arteries of the Circle of Willis is necessary [11].
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4.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 5, 2009, No. 1
,
,
,
Chronic thrombosis
of
the common and internal carotid arteries caused by confluent heterogenic plaques and collateral circulation through the external carotid arteries, the vertebral arteries and the posterior part
of
the
circle
of
Willis
were demonstrated by color-coded duplex scan.
Non-specific features and mild neurological and cognitive impairment were found by clinical examination. Modifiable risk factors for cerebrovascular diseases (arterial hypertension, hyperlipidemia and regular smoking) were registered. Hypertonic angiopathy with cholesterol emboli in the retinal vessels were seen by ophtalmoscopy.
Chronic thrombosis of the common and internal carotid arteries caused by confluent heterogenic plaques and collateral circulation through the external carotid arteries, the vertebral arteries and the posterior part of the circle of Willis were demonstrated by color-coded duplex scan.
A good correlation between the neurosonographic and angiographic findings was established. Focal leucoencephalopathy and ventriculomegaly were detected by MRI. Irregular alpha rhythm from the parietooccipital regions and mild intraocular asymmetry with relatively prolonged P 100 latency on the right side were registered electrophysiologically.
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5.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 2
,
,
,
The latter comprises
of
course the
circle
of
Willis
.
This tutorial will cover the basic knowledge of the arterial blood supply of the brain. The extracranial anterior and posterior system, i.e. the carotid and the vertebral arteries will be discussed as well as the intracranial arteries. Special attention will be paid to the concept of endarteries versus collateral blood supply.
The latter comprises of course the circle of Willis.
Also, there will be a short reflection on the anatomical properties of the vessel wall, which are the prerequisite for their functional behaviour.
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blood vessels, cerebral circulation,
circle
of
Willis
.
blood vessels, cerebral circulation, circle of Willis.
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6.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 2
,
,
,
A complete
circle
of
Willis
and the possibility to activate primary collaterals (anterior communicating artery, posterior communicating artery) or secondary collaterals (ophthalmic artery, leptomeningeal arteries) reduces the risk
of
hemodynamic ischemic stroke.
Once the anatomical diagnosis of an intracranial stenosis is made, it is crucial to understand the functional significance and the hemodynamic effects of the stenosis. Transcranial ultrasound can surely help by studying collaterals, testing for vasomotor reactivity and detecting emboli. In fact TCD/TCCS can provide real-time information on collateral flow and in case of vessel obstruction, activation of collateral pathways is very important for the clinical outcome of the patient.
A complete circle of Willis and the possibility to activate primary collaterals (anterior communicating artery, posterior communicating artery) or secondary collaterals (ophthalmic artery, leptomeningeal arteries) reduces the risk of hemodynamic ischemic stroke.
Sometimes we see a compensatory increase of blood flow velocity in the donor vessel due to recruitment of collaterals by vasodilation in tissues with compromised perfusion. This is called flow diversion and represents a natural steal by vessels distal to an arterial occlusion.
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7.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 2
,
,
,
The fetal variant
of
the
circle
of
Willis
and its influence on the cerebral collateral circulation.
Van Raamt AF, Mali WPTM, van Laar PJ, van der Graaf Y.
The fetal variant of the circle of Willis and its influence on the cerebral collateral circulation.
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To describe a patient with Moyamoya disease as a progressive, occlusive disease
of
the cerebral vessels with particular involvement
of
the
circle
of
Willis
and its feeding arteries.
To describe a patient with Moyamoya disease as a progressive, occlusive disease of the cerebral vessels with particular involvement of the circle of Willis and its feeding arteries.
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8.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 1
,
,
,
41 patients with severe stenosis and 30 patients with occlusion
of
ICA underwent brain MRT, 3D TOF-MR-angiography, Color Doppler
of
extraand intracranial vessels to investigate collateral flow via the
circle
of
Willis
and via the ophthalmic artery (OphA).
41 patients with severe stenosis and 30 patients with occlusion of ICA underwent brain MRT, 3D TOF-MR-angiography, Color Doppler of extraand intracranial vessels to investigate collateral flow via the circle of Willis and via the ophthalmic artery (OphA).
Maps of the cerebral perfusion parameters were calculated.
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Thirteen patients (85%) without collateral flow via the
circle
of
Willis
or flow via the PComA only have a higher incidence
of
brain infarction and impaired hemodynamic parameters in the MCA (V mean-38cm/s, PI-0.69), than patients with collateral flow via the AComA (2 infarctions, Vmean-44cm/s, PI-0.77).
In 50 (70%) cases “symptomatic” cerebral ischemia was noted. In symptomatic patients cortical middle cerebral artery (MCA) infarctions – 13 (26%), and border-zone infarctions – 10 (20%) prevailed. In cases of unilateral ICA occlusion compensatory dilatation of contralateral ICA and enhancement of flow volume by 60%, additional enhancement of the flow in vertebral arteries by 18% was observed.
Thirteen patients (85%) without collateral flow via the circle of Willis or flow via the PComA only have a higher incidence of brain infarction and impaired hemodynamic parameters in the MCA (V mean-38cm/s, PI-0.69), than patients with collateral flow via the AComA (2 infarctions, Vmean-44cm/s, PI-0.77).
Patients with reversed OphA could prove an additional risk for infarction.
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The primary collateral pathway is the
circle
of
Willis
, with the possibility
of
redistributing flow from the contralateral ICA via the anterior communicating artery or from the vertebrobasilar arteries via the posterior communicating artery.
In patients with occlusive disease of the internal carotid artery (ICA), collateral circulation is important to maintain adequate cerebral perfusion.
The primary collateral pathway is the circle of Willis, with the possibility of redistributing flow from the contralateral ICA via the anterior communicating artery or from the vertebrobasilar arteries via the posterior communicating artery.
Secondary collateral pathways include the external carotid artery via the ophthalmic artery and leptomeningeal anastomoses at the brain surface. When these collateral pathways are not adequate to maintain normal blood flow, vasodilatation of arterioles occurs and reduces cerebrovascular resistance for sustaining normal cerebral perfusion [1–3].
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All patients underwent a careful neurological and cardiological examination, ECG, transthoracic echocardiography, brain MRT, 3D TOF-MRangiography, Color Doppler
of
extraand intracranial vessels to investigate collateral flow via the
circle
of
Willis
: anterior communicating (AComA) and posterior communicating (PComA) arteries, and via the ophthalmic artery (OA).
All patients underwent a careful neurological and cardiological examination, ECG, transthoracic echocardiography, brain MRT, 3D TOF-MRangiography, Color Doppler of extraand intracranial vessels to investigate collateral flow via the circle of Willis: anterior communicating (AComA) and posterior communicating (PComA) arteries, and via the ophthalmic artery (OA).
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Examination
of
vessels
of
the
circle
of
Willis
was performed as described by Aaslid et al.
Examination of vessels of the circle of Willis was performed as described by Aaslid et al.
Blood flow velocities (V – cm/s) in the middle, anterior, posterior cerebral arteries (MCA, ACA, PCA) and pulsatile indexes (PI) were measured. The patency of major collateral vessels, namely OA, anterior (ACoA), and posterior (PCoA) communicating arteries, was evaluated.
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To assess the collateral flow in the
circle
of
Willis
we studied the presence and character
of
collateral flow in the so-called primary pathwayvia anterior communicating artery (AComA) and secondary pathwayvia ophthalmic artery (OA) (Table 2).
To assess the collateral flow in the circle of Willis we studied the presence and character of collateral flow in the so-called primary pathwayvia anterior communicating artery (AComA) and secondary pathwayvia ophthalmic artery (OA) (Table 2).
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Circle
of
Willis
/ Вилизиев кръг
Circle of Willis / Вилизиев кръг
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We found that patients without collateral flow via the
circle
of
Willis
or flow via the PComA only (n=15) have a high incidence
of
brain infarction.
We found that patients without collateral flow via the circle of Willis or flow via the PComA only (n=15) have a high incidence of brain infarction.
Despite that in 11 (71%) cases PComA was patent, in 13 (85%) patients presence of infarction was noted: 8 (53%) border-zone and 5 (33%) cortical infarctions of the MCA supply area. TCCD showed significant decrease of flow in the MCA (V mean38cm/s, PI-0.69) in this group.
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In order to assess the
circle
of
Willis
anatomy all patients underwent 3D-time-
of
-flight (TOF) MRangiography.
In order to assess the circle of Willis anatomy all patients underwent 3D-time-of-flight (TOF) MRangiography.
Investigation revealed the presence of classic circle of Willis in 38 (54%) patients; however, it must be mentioned, that in 10 cases one of the PComA was projected by thin (0.8–1.2 mm) line and
read the entire text >>
Investigation revealed the presence
of
classic
circle
of
Willis
in 38 (54%) patients; however, it must be mentioned, that in 10 cases one
of
the PComA was projected by thin (0.8–1.2 mm) line and
In order to assess the circle of Willis anatomy all patients underwent 3D-time-of-flight (TOF) MRangiography.
Investigation revealed the presence of classic circle of Willis in 38 (54%) patients; however, it must be mentioned, that in 10 cases one of the PComA was projected by thin (0.8–1.2 mm) line and
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Competent (closed)
circle
of
Willis
; MR-angiography, gad-fl3d-tof-MIP,
Competent (closed) circle of Willis; MR-angiography, gad-fl3d-tof-MIP,
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Noncompetent
circle
of
Willis
; MR-angiography, gad-fl3d-tof-MIP; right AComA and left PComA are absent.
Noncompetent circle of Willis; MR-angiography, gad-fl3d-tof-MIP; right AComA and left PComA are absent.
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Distribution
of
Cerebral Blood Flow in the
Circle
of
Willis
.
Hendrikse J, Van Raamt AF, Van der Graaf Y, Mali WP, van der Grond J.
Distribution of Cerebral Blood Flow in the Circle of Willis.
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9.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 14, 2018, No. 2
,
,
,
the
circle
of
Willis
.
the circle of Willis.
These communicating arteries are very important since they function immediately according to the pressure gradients. In contrast with the primary collaterals, development of secondary collateral circulation takes time. The most common secondary collateral pathway is formed by the periorbital vessels that connect the branches of the external and internal carotid arteries.
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If the
circle
of
Willis
is complete, the communicating arteries may compensate the pressure changes, i.e.
If the circle of Willis is complete, the communicating arteries may compensate the pressure changes, i.e.
severe carotid stenosis is not associated with decrease of perfusion pressure in this case. Since the perfusion pressure does not change, arterioles will not dilate compensatory, therefore application of vasodilative stimuli (e.g. CO
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However, the
circle
of
Willis
is often not complete, therefore the communicating arteries cannot compensate the effect
of
the carotid stenosis in this case.
) results in increase of diameter of these vessels, leading to increase in cerebral blood flow and flow velocity (Fig. 2).
However, the circle of Willis is often not complete, therefore the communicating arteries cannot compensate the effect of the carotid stenosis in this case.
If the collateral circulation does not function properly, severe carotid stenosis results in decrease in perfusion pressure. In response to
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10.
NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 15, 2019, No. 1
,
,
,
Distally the internal carotid and vertebral arteries are patent, without significant stenoses and dilatations up to the level
of
the
circle
of
Willis
.
The CTA of the main neck vessels, performed on a 64 Slices Toshiba Aquilion machine displays bilateral aneurysms of the common carotid arteries along their entire length, with asymmetric circular thromboses in their upper halves. High-grade short segment stenoses of the internal carotid and vertebral arteries in their proximal segments are seen.
Distally the internal carotid and vertebral arteries are patent, without significant stenoses and dilatations up to the level of the circle of Willis.
Thickening of the wall of the thoracic aorta at the level of the arc is found as well (Fig. 1).
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The thoracoabdominal aneurysm and the
circle
of
Willis
are also imaged.
MIP and VRT reconstructions of the MRA. The diameter and the extension of the aneurysms are identical with those on CTA. A larger segment of the aorta is covered.
The thoracoabdominal aneurysm and the circle of Willis are also imaged.
The thoracic aorta is dilated along its entire length, maximally in its thoraco-abdominal segment – up to 3.65 cm.
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The internal carotid artery on the left is poorly filled along its entire length up to the
circle
of
Willis
(Fig. 5).
The patient is referred to Rheumatology Clinic for therapy, where immunological tests confirm Takayasu decease. After a three-month treatment (immunosuppressive therapy and corticosteroids) and normalization of immunological markers, a follow-up CTA shows a complete thrombosis of the aneurysm of the left common carotid artery and a collateral filling of the internal carotid artery at the left via the ipsilateral external carotid artery.
The internal carotid artery on the left is poorly filled along its entire length up to the circle of Willis (Fig. 5).
At the right no differences with the previous imaging results are seen.
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